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Step 1 (Steffanie) > Endocrine Pharm > Flashcards

Endocrine Pharm Flashcards

1
Q

Name the rapid acting insulin preparations

A

Lispro, Aspart, Glulisine

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2
Q

MOA of insulin

A

Bind insulin receptor (tyrosine kinase activity). Liver: Increase glucose stored as glycogen. Muscle: Increase glycogen, protein synthesis. Fat: Increase TG storage. Cell membrane: Increase K+ uptake

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3
Q

Adverse effects of insulin

A

Hypoglycemia, lipodystrophy, rare hypersensitivity reactions

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4
Q

Short acting insulin

A

Regular insulin

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5
Q

Intermediate acting insulin

A

NPH

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6
Q

Long acting insulin

A

Detemir, glargine

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7
Q

MOA of Amylin analogs

A

Decrease glucagon release, decrease gastric acid emptying, increase satiety

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8
Q

Name the Amylin analog

A

Pramlintide

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9
Q

MOA of GLP-1 analogs

A

Decrease glucagon release, decrease gastric emptying, increase glucose dependent insulin release, increase satiety

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10
Q

Name the GLP-1 analogs

A

Exenatide, liragtutide

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11
Q

What are adverse effects of GLP-1 analogs?

A

Nausea, vomiting, pancreatitis. Promote weight loss (often desired)

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12
Q

MOA of Biguanides

A

Inhibit hepatic gluconeogenesis and the action of glucagon, by inhibiting mGPD. Increase glycolysis, peripheral glucose uptake (increase insulin sensitivity)

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13
Q

What category of drugs is Metformin?

A

Biguanide

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14
Q

Adverse effects of Metformin?

A

GI upset, lactic acidosis (use with caution in renal insufficiency), B12 deficiency. Promote weight loss (often desired).

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15
Q

What are the 1st generation sulfonylureas?

A

Chlorpropamide, tolbutamide

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16
Q

What are the 2nd generation sulfonylureas?

A

Glimepiride, glipizide, gylburide

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17
Q

MOA of sulfonylureas

A

Close K+ channel in pancreatic beta cell membrane, leads to cell depolarizing, insulin release via increase Ca2+ influx

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18
Q

Name the Meglitinides

A

Nateglinide, repaglinide

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19
Q

MOA of meglitinides

A

Close K+ channel in pancreatic beta cell membrane, leads to cell depolarizing, insulin release via increase Ca2+ influx (binding site differs from sulfonylureas)

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20
Q

Name the DPP-4 inhibitors

A

Linagliptin, saxagliptin, sitagliptin

21
Q

MOA of DPP-4 inhibitors

A

Inhibit DPP-4 enzyme that deactivates GLP-1. Decrease glucagon release, gastric emptying. Increase glucose-dependent insulin release, satiety.

22
Q

Side effects of DPP-4 inhibitors

A

Mild urinary or respiratory infections, weight neutral

23
Q

Name the Glitazones/thiazolidinediones

A

Pioglitazone, rosiglitazone

24
Q

MOA of glitazones/thiazolidinediones

A

Binds to PPAR-gamma nuclear transcription regulator, which increases insulin sensitivity and levels of adiponectin, leads to regulation of glucose metabolism and fatty acid storage

25
Q

Adverse effects of glitazones/thiazolidinediones

A

Weight gain, edema, HF, increased risk of fractures. Delated onset of action (several weeks). Not used in HF pts

26
Q

Name the SGLT2 inhibitors

A

Canagliflozin, dapagliflozin, empagliflozin

27
Q

MOA of SGLT2 inhibitors

A

Block reabsorption of glucose in proximal convoluted tubule

28
Q

Adverse effects of SGLT2 inhibitors

A

Glucosuria, UTIs, vaginal yeast infections, hyperkalemia, dehydration, weight loss

29
Q

Name the alpha-glucosidase inhibitors

A

Acarbose, miglitol

30
Q

MOA of alpha-glucosidase inhibitors

A

Inhibit intestinal brush border alpha-glucosidases, leads to delayed carbohydrate hydrolysis and glucose absorption, which leads to decreased postprandial hyperglycemia

31
Q

Name the Thioamides

A

Propylthiouricil, methimazole

32
Q

MOA of Thioamides

A

Block thyroid peroxidase, inhibiting the oxidation of iodine and the organification and coupling of iodine, leading to inhibition of thyroid hormone synthesis.
PTU also blocks 5’-deiodinase and leads to decreased peripheral converstion of T4 to T3.

33
Q

Clinical use of Thioamides

A

Hyperthyroidism

34
Q

Adverse effects of Thioamides

A

Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity.

35
Q

What can Methimazole cause if taken during pregnancy?

A

Aplasia cutis

36
Q

Clinical use of ADH antagonists

A

SIADH, block action of ADH at V2-receptor

37
Q

Clinical use of Desmopressin

A

Central (not nephrogenic) DI, von Willebrand disease, sleep enuresis, hemophilia A

38
Q

GH clinical uses

A

GH deficiency, Turner syndrome

39
Q

Oxytocin clinical uses

A

Labor induction, milk letdown; controls uterine hemorrhage

40
Q

Somatostatin (octreotide) clinical uses

A

Acromegaly, carcinoid syndrome, gastrinoma, glucagonoma, esophageal varices

41
Q

MOA of Demeclocycline

A

ADH antagonist

42
Q

Clinical use of Demeclocycline

A

SIADH

43
Q

MOA of Fludrocortisone

A

Synthetic analog of aldosterone with little glucocorticoid effects

44
Q

Clinical use of Fludrocortisone

A

Mineralocorticoid replacement in primary adrenal insufficiency

45
Q

MOA of Cinacalcet

A

Sensitizes Ca2+-sensing receptors (CaSR) in parathyroid gland to circulating Ca2+, leading to decreased PTH

46
Q

Clinical use of Cinacalcet

A

Refractory hypercalcemia in primary hyperparathyroidism, secondary hyperparathyroidism, or parathyroid carcinoma

47
Q

MOA of Sevelamer

A

Nonabsorable phosphate binder that prevents phosphate absorption from the GI tract

48
Q

Clinical use of Sevelamer

A

Hyperphosphatemia in CKD

Step 1 (Steffanie) (21 decks)

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